Laparoscopic Cholecystectomy for Gallbladder Calculosis in Fibromyalgia Patients: Impact on Musculoskeletal Pain, Somatic Hyperalgesia and Central Sensitization.

Raffaele Costantini,Paolo Innocenti,Francesca Massimini,Claudio Tana,Maria Adele Giamberardino,Giannapia Affaitati,Theodore John Price

doi:10.1371/journal.pone.0153408

Raffaele Costantini, Paolo Innocenti + Show 5 more

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https://doi.org/10.1371/journal.pone.0153408

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Abstract

Fibromyalgia, a chronic syndrome of diffuse musculoskeletal pain and somatic hyperalgesia from central sensitization, is very often comorbid with visceral pain conditions. In fibromyalgia patients with gallbladder calculosis, this study assessed the short and long-term impact of laparoscopic cholecystectomy on fibromyalgia pain symptoms. Fibromyalgia pain (VAS scale) and pain thresholds in tender points and control areas (skin, subcutis and muscle) were evaluated 1week before (basis) and 1week, 1,3,6 and 12months after laparoscopic cholecystectomy in fibromyalgia patients with symptomatic calculosis (n = 31) vs calculosis patients without fibromyalgia (n. 26) and at comparable time points in fibromyalgia patients not undergoing cholecystectomy, with symptomatic (n = 27) and asymptomatic (n = 28) calculosis, and no calculosis (n = 30). At basis, fibromyalgia+symptomatic calculosis patients presented a significant linear correlation between the number of previously experienced biliary colics and fibromyalgia pain (direct) and muscle thresholds (inverse)(p<0.0001). After cholecystectomy, fibromyalgia pain significantly increased and all thresholds significantly decreased at 1week and 1month (1-way ANOVA, p<0.01-p<0.001), the decrease in muscle thresholds correlating linearly with the peak postoperative pain at surgery site (p<0.003-p<0.0001). Fibromyalgia pain and thresholds returned to preoperative values at 3months, then pain significantly decreased and thresholds significantly increased at 6 and 12months (p<0.05-p<0.0001). Over the same 12-month period: in non-fibromyalgia patients undergoing cholecystectomy thresholds did not change; in all other fibromyalgia groups not undergoing cholecystectomy fibromyalgia pain and thresholds remained stable, except in fibromyalgia+symptomatic calculosis at 12months when pain significantly increased and muscle thresholds significantly decreased (p<0.05-p<0.0001). The results of the study show that biliary colics from gallbladder calculosis represent an exacerbating factor for fibromyalgia symptoms and that laparoscopic cholecystectomy produces only a transitory worsening of these symptoms, largely compensated by the long-term improvement/desensitization due to gallbladder removal. This study provides new insights into the role of visceral pain comorbidities and the effects of their treatment on fibromyalgia pain/hypersensitivity.

Highlights

Fibromyalgia is a chronic pain syndrome affecting 4–7% of the general population, prevalently women [1]
Its diagnostic criteria were first introduced by the American College of Rheumatology (ACR) in 1990 [2]: (1) presence of diffuse musculoskeletal pain of at least 3 months’ duration; (2) positivity of at least 11 out of 18 specific body sites called tender points (TePs), i.e., exquisite tenderness elicited at these points with a standard pressure of 4 kg-f exerted either manually or measured via a pressure algometer
In fibromyalgia patients with symptomatic gallbladder calculosis with respect to fibromyalgia patients with asymptomatic gallbladder calculosis and without gallbladder pathology: Visual Analogue Scale (VAS) of FMS pain was significantly higher and pressure pain thresholds (PPTs) in TePs were lower, the difference being significant for FMS+sGb +Cholec and FMS+sGb vs FMS (Table 1)

Summary

Introduction

Fibromyalgia is a chronic pain syndrome affecting 4–7% of the general population, prevalently women [1]. The pathophysiology of fibromyalgia is still under investigation; knowledge so far acquired, indicates that a key role in the syndrome is played by phenomena of central amplification of pain signals, due to an imbalance of neurotransmitters involved in nociceptive transmission/control in the Central Nervous System (CNS), in genetically predisposed individuals [1,8,9]. In spite of the basically central nature of the syndrome, the role of peripheral conditions as possible pain exacerbating factors in FMS has being increasingly recognized in recent years, with nociceptive inputs from the periphery enhancing the level of central sensitization and the extent of pain symptoms/ hypersensitivity typical of the syndrome [7,11,12]

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